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PNAS | March 13, 2001 | vol. 98 | no. 6 | 3369-3374
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Medical Sciences
 The nuclear receptor PXR is a lithocholic acid sensor that protects against liver toxicity

Jeff L. Staudinger*,dagger , Bryan Goodwin*, Stacey A. Jones*, Diane Hawkins-BrownDagger , Kathleen I. MacKenzie§, Anne LaTour, Yaping Liu||, Curtis D. Klaassen||, Kathleen K. Brown**, John Reinhard§, Timothy M. Willsondagger dagger , Beverly H. Koller, and Steven A. Kliewer*,Dagger Dagger

Departments of * Molecular Endocrinology, Dagger  Bioscience Support, § Molecular Pharmacology, ** Metabolic Diseases, and dagger dagger  Medicinal Chemistry, GlaxoSmithKline, Research Triangle Park, NC 27709;  Curriculum in Genetics, Department of Medicine, University of North Carolina, Chapel Hill, NC 27599; and || Department of Pharmacology and Toxicology, University of Kansas Medical Center, Kansas City, KS 66160

Edited by Ronald W. Estabrook, University of Texas Southwestern Medical Center, Dallas, TX, and approved January 4, 2001 (received for review November 22, 2000)

The pregnane X receptor (PXR) is the molecular target for catatoxic steroids such as pregnenolone 16alpha -carbonitrile (PCN), which induce cytochrome P450 3A (CYP3A) expression and protect the body from harmful chemicals. In this study, we demonstrate that PXR is activated by the toxic bile acid lithocholic acid (LCA) and its 3-keto metabolite. Furthermore, we show that PXR regulates the expression of genes involved in the biosynthesis, transport, and metabolism of bile acids including cholesterol 7alpha -hydroxylase (Cyp7a1) and the Na+-independent organic anion transporter 2 (Oatp2). Finally, we demonstrate that activation of PXR protects against severe liver damage induced by LCA. Based on these data, we propose that PXR serves as a physiological sensor of LCA, and coordinately regulates gene expression to reduce the concentrations of this toxic bile acid. These findings suggest that PXR agonists may prove useful in the treatment of human cholestatic liver disease.

dagger Current address: Department of Pharmacology and Toxicology, University of Kansas Medical Center, Kansas City, KS 66160.

Dagger Dagger To whom reprint requests should be addressed at: GlaxoSmithKline, Room V118, Five Moore Drive, Research Triangle Park, NC 27709. E-mail: sak15922{at}glaxowellcome.com.

www.pnas.org/cgi/doi/10.1073/pnas.051551698
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